REVIEW: Interaction Between Adipocytes and B Lymphocytes in Human Metabolic Diseases

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Ekaterina M. Stasevich¹, Elina A. Zheremyan¹, Dmitriy V. Kuprash¹, and Anton M. Schwartz^1,2,3,a*

¹Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia

²Moscow Institute of Physics and Technology, 141701 Moscow, Russia

³Department of Human Biology, University of Haifa, Haifa, Israel

^* To whom correspondence should be addressed.

Received December 20, 2022; Revised January 25, 2023; Accepted February 2, 2023

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Diseases associated with the disorders of carbohydrate and lipid metabolism are widespread in the modern world. Interaction between the cells of adipose tissue – adipocytes – and immune system cells is an essential factor in pathogenesis of such diseases. Long-term increase in the glucose and fatty acid levels leads to adipocyte hypertrophy and increased expression of pro-inflammatory cytokines and adipokines by these cells. As a result, immune cells acquire a pro-inflammatory phenotype, and new leukocytes are recruited. Inflammation of adipose tissue leads to insulin resistance and stimulates formation of atherosclerotic plaques and development of autoimmunity. New studies show that different groups of B lymphocytes play an essential role in regulation of adipose tissue inflammation. Decrease in the number of B-2 lymphocytes suppresses development of a number of metabolic diseases, whereas decreased numbers of the regulatory B lymphocytes and B-1 lymphocytes are associated with more severe pathology. Recent studies showed that adipocytes influence B lymphocyte activity both directly and by altering activity of other immune cells. These findings provide better understanding of the molecular mechanisms of human pathologies associated with impaired carbohydrate and lipid metabolism, such as type 2 diabetes mellitus.

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KEY WORDS: B lymphocytes, B1 lymphocytes, B2 lymphocytes, regulatory B lymphocytes, adipocytes, adipokines, diabetes

DOI: 10.1134/S0006297923020104

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